Grant: Fellowship: Prize of Excellence in Research on Aging
Direct Payment
$5,000.00
Cellular Stress Responses in Microglia Biology and Neurodegeneration
FY 2013-14
Summary
Microglia, the resident immune cells of central nervous system (CNS), help maintain CNS homeostasis by mediating the phagocytosis and clearance of debris. Conversely, inflammatory cytokines and chemokines secreted by these cells, in conjunction with CNS-homing monocytes and macrophages, have been shown to aggravate the time of onset and severity of chronic neurodegenerative diseases such as Alzheimer's disease (AD) and Amyotrophic Lateral Sclerosis (ALS). Here, I am proposing a project that aims to determine how the conserved cellular stress response, a pathway that has been shown to be strongly upregulated during acute and chronic neuronal injury, regulates the inflammatory capacity of microglia and CNS-invading inflammatory monocytes. Moreover, I will determine the role of this response during the pathogenesis of AD and ALS in established animal models. This work will have an important impact on increasing our knowledge on the pathogenesis of neurodegeration to identify novel pathways that can be targeted with therapeutics.
Department
Program
Fellowship: Prize of Excellence in Research on Aging
Recipient
Location
Massachusetts, United States of America
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
308825
Name
Rubino Stephen
Region
Massachusetts
Country
United States of America
Orgtype
Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Fellowships - Post-PhD
Projecttitle
Cellular Stress Responses in Microglia Biology and Neurodegeneration
Programtype2
Fellowship Programs
Orgnameinp2
Direct Payment
Cihramount2
$5,000
Cihrequipment2
$0
Programname2
Fellowship: Prize of Excellence in Research on Aging
Keyworddelim
Alzheimer'S Disease; Amyotrophic Lateral Sclerosis; Cellular Stress; Innate Immunity; Microglia; Neuroinflammation
Abstract
Microglia, the resident immune cells of central nervous system (CNS), help maintain CNS homeostasis by mediating the phagocytosis and clearance of debris. Conversely, inflammatory cytokines and chemokines secreted by these cells, in conjunction with CNS-homing monocytes and macrophages, have been shown to aggravate the time of onset and severity of chronic neurodegenerative diseases such as Alzheimer's disease (AD) and Amyotrophic Lateral Sclerosis (ALS). Here, I am proposing a project that aims to determine how the conserved cellular stress response, a pathway that has been shown to be strongly upregulated during acute and chronic neuronal injury, regulates the inflammatory capacity of microglia and CNS-invading inflammatory monocytes. Moreover, I will determine the role of this response during the pathogenesis of AD and ALS in established animal models. This work will have an important impact on increasing our knowledge on the pathogenesis of neurodegeration to identify novel pathways that can be targeted with therapeutics.
Competitiondate
201311
Approvedterm2
1 yr 0 mth
Pinamesdelim
Rubino, Stephen
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $5,000~ $0~